The cornea provides special advantages over other body structures of the study of immunological and inflammatory reactions in vivo: It is avascular, it is transparent and it possesses a relatively acellular stromal matrix of multilamellar collagen fibrils. Structurally it resembles the endothelial-lined wall of an artery. Furthermore, localized events instigated in one cornea do not influence the behavior of the contralateral cornea. This permits experiments where one eye of the same animal may serve as a control. In addition, corneal avascularity is responsible for very slow diffusion or escape kinetics of injected macromolecular species. In the present study we will examine the behavior of the cornea to a carefully selected group of antigens and inflammatory stimulants permitting us to separate and identify individual immunogenic activities. Some of these agents will include certain microbial antigens which can induce a specific immunogenic response to T or B lymphocytes. The Wessely phenomenon and related corneal responses to these antigens will be examined for the specific cellular and humoral components that they elicit. These events will be related to the mechanisms involved in the development of transient and permanent corneal opacities whether they be of milder edematous form of herpesvirus disciform keratitis or the more severe forms of deep stromal ulceration. Stromal ulceration induced by foreign substances but mediated by host polymorphonuclear leukocytes, will also be studied. The overall goal will be to determine how corneal opacities occur, how the cornea develops resistance to infection, and how these processes might be controlled to prevent blindness.